Orthostatic Hypotension

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    Intro

    • Defined as:
      • reduction in sBP >20
        OR
      • reduction in dBP >10
    • Classic manifestation of sympathetic vasoconstrictor (autonomic) failure.
    • Three types:
      • 1. No compensatory ↑ in HR, despite ↓ BP.
      • 2. HR may ↑, but not sufficiently to maintain BP
        • Mild autonomic failure.
      • 3. Delayed orthostatic hypotension (after >3min of standing)
        • Mild/early sympathetic adrenergic dysfunction.
      • 4. Hypotension within 15s of standing
        • Mismatch of cardiac output and peripheral vascular disease (not autonomic failure).
    • Worsens with age:
      • Decreased baroreflex responsiveness
      • Decreased cardiac compliance
      • Less vestibulosympathetic reflex.
    • Prevalence 54-68% in care facilities, and about 6% in community.

     

    Mechanism

    • Standing causes pooling of 500-1000mL of blood in lower extremities and splanchnic circulation.
    • Decrease in venous return -->
      • Reduced ventricular filling -->
        • reduced cardiac output + BP -->
    • Compensatory response:
      • Baroreceptors in carotid sinus + aortic arch detect change -->
        • increased sympathetic flow and decreased vagal activity-->
              1. Increases peripheral vascular resistance --> increasing return to heart
              2. Increases cardiac output
    • If BP fails to rise:
      • --> orthostatic hypotension and cerebral hypoperfusion occur.
    • Symptoms:
      • Generalized, weakness, fatigue, nausea, cognitive slowing, headache.
      • Visual blurring (retinal/occipital ischemia)
      • Neck pain (muscle hypoperfusion)
      • Orthostatic dyspnea (VQ mismatch in lungs, decreased perfusion)
      • Angina (impaired myocardial perfusion, even if normal coronaries).
         
    • OrthostaticHypotensionPictureNEJm.png

     

    Causes

    • Hemodynamic
      • Hypovolemia
      • Antihypertensives
      • Decreased cardiac output
        • Constrictive pericarditis
        • Cardiomyopathy
        • Aortic stenosis
      • Endocrine
        • Adrenal insufficiency
        • Pheochromocytoma
        • Excessive vasodilatation (systemic mastocytosis and carcinoid syndrome)
      • Harnesses (climbing)
    • Neurogenic Dysfunction
      • Medication:
        • Psych:
          • Antidepressants
          • Tricyclics
          • MAOI's
        • Vasodilators:
          • a-1 blockers (inhibit vasoconstriction by baroreceptor reflex)

     

    Treatments

    • Discontinue offending medications
    • B-blockers generally do not cause profound orthostatic hypotension
    • Alpha-Blockers are main culprits
      • Avoid Doxasozin and Terazosin (less selective for prostate, worse symptoms)
      • Tamsulosin, Alfuzosin are better, but still cause orthostatic hypotension. 

    Non-Pharmacologic

    Group Intervention Comments
    Decrease sudden changes Perform gradual staged movements with postrual change Tiem should be allowed for autonomic adaptation
      Avoid prolongued immobilization Deconditioning exacerbates orthostatic hypotension

    Decrease blood pooling

    /

    Improve venous return

    Perform physical maneuvers to decrease blood pooling

    (Crossing legs, stooping, squatting, and tensing muscles)

    Decrease peripheral pooling, increase venous return to heart
    Wear custom-fitted elastic stockings and abdominal binder Reduces peripheral pooling in limbs and splanchnic circulation
    Avoid straining, coughing, and other maneuvers that increase interthoracic pressure Inhibit venous return to the heart, decreasing cardiac output.
    Allow Hypertension Discontinue hypotensive and antihypertensive medications May be necessary to allow some supine hypertension.
    Increase fluid/salt intake Recommended 2.0-2.5 L/day of fluid or 10g sodium.
    Drink water rapidly 500mL of tap water raises BP in 5-15min for 1h.
    Raise head of bed by 10-20 degrees

    Minimizes pressure diuresis during sleep

    Supine hypertension --> nocturnal pressure diuresis

     

    Pharmacologic

    Agent Class Mechanism Notes
    Fludrocortisone Acetate Mineralcorticoid Fluid and sodium retention

    Most OrthoHypotension is neurogenic,

    this is only of limited effectiveness, but often used.

    - If there is a adrenal insufficiency

    - If cannot increase plasma volume w/ salt + water.

    Midodrine

    (Mean of

    8.4mg TID used in trial)

    Alpha1-adrenoreceptor

    agonist

    Increases peripheral vascular resistance

    - Only one approved by FDA for ortho-hypoBP

    - Double blind, placebo-ctld, multi-ctr trial:

    Significantly increased standing BP and reduced symptoms.

    - Compared with ephedrine (midodrine is better)

    Desmopressin acetate DDAVP Volume expansion, reduce nocturnal diuresis.

    - Useful for autonomic failure secondary to neurodegenerative process (loss of vasopressor neurons)

    Erythropoietin Erythropoietin

    1. Increases RBC mass and central blood volume

    2. Increases blood viscocity

    3. Vascular neurohumoral effects

    - Use if orthostatic hypo-BP and anemia.

    - Controlled Trial (NEJM 1993): Improves orthostatic tolerance (controlled trial) if orthostatic BP and anema

     

    Pyridostigmine ACh Esterase Inhibitor

    - Inhibition of ACh Esterase enhances sympathic transmission

    - Effect maximal if upright b/c this

    is the point of maximal sympathetic transmission.

    - Little to no increase in supine BP

    - Controlled trials: modest increase in BP in pts with neurological orthostatic hypo-BP.

    Others:

    COX inhibitors

    B-antagonists

    Clonidine

    yohimbine

    Somatostatin

    Dihydroergotamine

    Dopamine Agonists

    - Inconsistent results based on may trials (see ref below)
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